Secondary hyperparathyroidism (sHPT), i.e. the over-production of parathyroid hormone (PTH) by the parathyroid glands, affects the majority of untreated end-stage renal failure patients. If this condition is untreated, it leads to bone pain, fractures, cognitive impairment and depression, thus reducing the quality of life of and increasing mortality of such patients. It is also associated with hypercalcaemia and higher arterial calcification scores, and it is an independent cardiovascular risk factor in itself. As early as stage II in the course of renal insufficiency, PTH levels start to rise with the declining ability of the kidneys to excrete phosphorus. In addition to this, with the declining ability of the kidneys to hydroxylate 25-OH Vitamin D3, levels of the potent PTH suppressor 1,25-OH Vitamin D3 fall below normal unless it is supplemented. In primary hyperparathyroidism (pHPT), PTH over-production occurs in adenomatous chief cells of the parathyroid glands without being triggered by renal insufficiency. If in the course of secondary HPT the glands lose their responsiveness to regulatory mechanisms, this is referred to as tertiary HPT.